Serial changes of serum IgE, IgG, eosinophils were observed in 25 patients with acute myocaridial infarction and 20 ischemic heart disease without evidence of acute myocardial infarction and evaluated in terms of several parameters and its clinical significance. The results observed were as follows : 1) Serum IgE levels were propgressively elevated from the first hospital day(259+/-3IU/ml) up to peak level of the fifth hospital day(415+/-2IU/ml) and progressively lowered and returned to almost same level as the first hospital day on the twenty first hospital day. On the other hand control group showed significantly lower IgE levels throughout all hospital day and also did not showed serial change. 2) In the patient group with the initial serum IgE level above 200IU/m; showed significantly lower level of serum SGOT, CPK level than the group of below 200IU/ml group. This suggests the initial serum IgE level might have some correlation of the extent of myocardial necrosis. 3) In patients of acute myocardial infarction, ejection fraction was checked at discharge. Initial serum IgE level above 200IU/ml group showed significantly higher ejection fraction than below 200IU/ml group(59.4+/-13.5% vs 38.4+/-13.7%). 4) Serum IgE was checked concomittantly with serum IgE. It showed slightly decreasing tendency at third hospital day but not statistically significant. Eosinophil changed similar pattern as serum IgE but it was also not statistically significant. In conclusion, serial checking of serum IgE level in patient of acute myocardial infarction may give some help in prediction the clinical course and prognosis.
Aspartate Aminotransferases ; Eosinophils ; Hand ; Humans ; Immunoglobulin E* ; Immunoglobulin G ; Immunoglobulins* ; Infarction ; Myocardial Infarction* ; Myocardial Ischemia ; Necrosis ; Prognosis

Amyloid-beta peptide (Abeta), generated by proteolytic cleavage of the amyloid precursor protein (APP), plays a pivotal role in the pathogenesis of Alzheimer's disease (AD). The key step in the generation of Abeta is cleavage of APP by beta-site APP-cleaving enzyme 1 (BACE1). Levels of BACE1 are increased in vulnerable regions of the AD brain, but the underlying mechanism is unknown. In the present study, we reported the effects of ferrous ions at subtoxic concentrations on the mRNA levels of BACE1 and a-disintegrin-and-metalloproteinase 10 (ADAM10) in PC12 cells and the cell responses to ferrous ions. The cell survival in PC12 cells significantly decreased with 0 to 0.3 mM FeCl2, with 0.6 mM FeCl2 treatment resulting in significant reductions by about 75%. 4,6-diamidino-2-phenylindole (DAPI) staining showed that the nuclei appeared fragmented in 0.2 and 0.3 mM FeCl2. APP-alpha-carboxyl terminal fragment (APP-alpha-CTF) associations with ADAM10 and APP-beta-CTF with BACE1 were increased. Levels of ADAM10 and BACE1 mRNA increased in response to the concentrations of 0.25 mM, respectively. In addition, p-ERK and p-Bad (S112, S155) expressions were increased, suggesting that APP-CTF formation is related to ADAM10/BACE1 expression. Levels of Bcl-2 protein were increased, but significant changes were not observed in the expression of Bax. These data suggest that ion-induced enhanced expression of AMDA10/BACE1 could be one of the causes for APP-alpha/beta-CTF activation.
Alzheimer Disease ; Amyloid ; Animals ; Brain ; Cell Survival ; Indoles ; Ions ; Iron ; PC12 Cells ; RNA, Messenger

In this study, we examined whether melatonin promotes apoptotic cell death via p53 in prostate LNCaP cells. Melatonin treatment significantly curtailed the growth of LNCaP cells in a dose- and time-dependent manner. Melatonin treatment (0 to 3 mM) induced the fragmentation of poly(ADP-ribose) polymerase (PARP) and activation of caspase-3, caspase-8, and caspase-9. Moreover, melatonin markedly activated Bax expression and decreased Bcl-2 expression in dose increments. To investigate p53 and p21 expression, LNCaP cells were treated with 0 to 3 mM melatonin. Melatonin increased the expressions of p53, p21, and p27. Treatment with mitogen-activated protein kinase (MAPK) inhibitors, PD98059 (ERK inhibitor), SP600125 (JNK inhibitor) and SB202190 (p38 inhibitor), confirmed that the melatonin-induced apoptosis was p21-dependent, but ERK-independent. With the co-treatment of PD98059 and melatonin, the expression of p-p53, p21, and MDM2 did not decrease. These effects were opposite to the expression of p-p53, p21, and MDM2 observed with SP600125 and SB202190 treatments. Together, these results suggest that p53-dependent induction of JNK/p38 MAPK directly participates in apoptosis induced by melatonin.
Anthracenes ; Apoptosis ; Caspase 3 ; Caspase 8 ; Caspase 9 ; Cell Death ; Flavonoids ; Imidazoles ; Melatonin ; Poly(ADP-ribose) Polymerases ; Prostate ; Protein Kinases ; Pyridines

Nociplastic pain by the “International Association for the Study of Pain” is defined as pain that arises from altered nociception despite no clear evidence of nociceptive or neuropathic pain. Augmented central nervous system pain and sensory processing with altered pain modulation are suggested to be the mechanism of nociplastic pain. Clinical criteria for possible nociplastic pain affecting somatic structures include chronic regional pain and evoked pain hypersensitivity including allodynia with after-sensation. In addition to possible nociplastic pain, clinical criteria for probable nociplastic pain are pain hypersensitivity in the region of pain to non-noxious stimuli and presence of comorbidity such as generalized symptoms with sleep disturbance, fatigue, or cognitive problems with hypersensitivity of special senses. Criteria for definitive nociplastic pain is not determined yet. Eight specific disorders related to central sensitization are suggested to be restless leg syndrome, chronic fatigue syndrome, fibromyalgia, temporomandibular disorder, migraine or tension headache, irritable bowel syndrome, multiple chemical sensitivities, and whiplash injury; non-specific emotional disorders related to central sensitization include anxiety or panic attack and depression. These central sensitization pain syndromes are overlapped to previous functional pain syndromes which are unlike organic pain syndromes and have emotional components. Therefore, nociplastic pain can be understood as chronic altered nociception related to central sensitization including both sensory components with nociceptive and/or neuropathic pain and emotional components. Nociplastic pain may be developed to explain unexplained chronic pain beyond tissue damage or pathology regardless of its origin from nociceptive, neuropathic, emotional, or mixed pain components.

One of the most common sources of spinal pain syndromes is the facet joints. Cervical, thoracic, and lumbar facet joint pain syndromes comprise 55%, 42%, and 31% of chronic spinal pain syndromes, respectively. Common facet joint disorders are degenerative disorders, such as osteoarthritis, hypertrophied superior articular process, and facet joint cysts; septic arthritis; systemic and metabolic disorders, such as ankylosing spondylitis or gout; and traumatic dislocations. The facet pain syndrome from osteoarthritis is suspected from a patient’s history (referred pain pattern) and physical examination (tenderness). Other facet joint disorders may cause radicular pain if mass effect from a facet joint cyst, hypertrophied superior articular process, or tumors compress the dorsal root ganglion.However, a high degree of morphological change does not always provoke pain. The superiority of innervating nerve block or direct joint injection for diagnosis and treatment is still a controversy. Treatment includes facet joint injection in facet joint osteoarthritis or whiplash injury provoking referred pain or decompression in mass effect in cases of hypertrophied superior articular process or facet joint cyst eliciting radicular pain. In addition, septic arthritis is treated using a proper antibiotic, based on infected tissue or blood culture. This review describes the diagnosis and treatment of common facet joint disorders.

Nociplastic pain by the “International Association for the Study of Pain” is defined as pain that arises from altered nociception despite no clear evidence of nociceptive or neuropathic pain. Augmented central nervous system pain and sensory processing with altered pain modulation are suggested to be the mechanism of nociplastic pain. Clinical criteria for possible nociplastic pain affecting somatic structures include chronic regional pain and evoked pain hypersensitivity including allodynia with after-sensation. In addition to possible nociplastic pain, clinical criteria for probable nociplastic pain are pain hypersensitivity in the region of pain to non-noxious stimuli and presence of comorbidity such as generalized symptoms with sleep disturbance, fatigue, or cognitive problems with hypersensitivity of special senses. Criteria for definitive nociplastic pain is not determined yet. Eight specific disorders related to central sensitization are suggested to be restless leg syndrome, chronic fatigue syndrome, fibromyalgia, temporomandibular disorder, migraine or tension headache, irritable bowel syndrome, multiple chemical sensitivities, and whiplash injury; non-specific emotional disorders related to central sensitization include anxiety or panic attack and depression. These central sensitization pain syndromes are overlapped to previous functional pain syndromes which are unlike organic pain syndromes and have emotional components. Therefore, nociplastic pain can be understood as chronic altered nociception related to central sensitization including both sensory components with nociceptive and/or neuropathic pain and emotional components. Nociplastic pain may be developed to explain unexplained chronic pain beyond tissue damage or pathology regardless of its origin from nociceptive, neuropathic, emotional, or mixed pain components.

One of the most common sources of spinal pain syndromes is the facet joints. Cervical, thoracic, and lumbar facet joint pain syndromes comprise 55%, 42%, and 31% of chronic spinal pain syndromes, respectively. Common facet joint disorders are degenerative disorders, such as osteoarthritis, hypertrophied superior articular process, and facet joint cysts; septic arthritis; systemic and metabolic disorders, such as ankylosing spondylitis or gout; and traumatic dislocations. The facet pain syndrome from osteoarthritis is suspected from a patient’s history (referred pain pattern) and physical examination (tenderness). Other facet joint disorders may cause radicular pain if mass effect from a facet joint cyst, hypertrophied superior articular process, or tumors compress the dorsal root ganglion.However, a high degree of morphological change does not always provoke pain. The superiority of innervating nerve block or direct joint injection for diagnosis and treatment is still a controversy. Treatment includes facet joint injection in facet joint osteoarthritis or whiplash injury provoking referred pain or decompression in mass effect in cases of hypertrophied superior articular process or facet joint cyst eliciting radicular pain. In addition, septic arthritis is treated using a proper antibiotic, based on infected tissue or blood culture. This review describes the diagnosis and treatment of common facet joint disorders.

Nociplastic pain by the “International Association for the Study of Pain” is defined as pain that arises from altered nociception despite no clear evidence of nociceptive or neuropathic pain. Augmented central nervous system pain and sensory processing with altered pain modulation are suggested to be the mechanism of nociplastic pain. Clinical criteria for possible nociplastic pain affecting somatic structures include chronic regional pain and evoked pain hypersensitivity including allodynia with after-sensation. In addition to possible nociplastic pain, clinical criteria for probable nociplastic pain are pain hypersensitivity in the region of pain to non-noxious stimuli and presence of comorbidity such as generalized symptoms with sleep disturbance, fatigue, or cognitive problems with hypersensitivity of special senses. Criteria for definitive nociplastic pain is not determined yet. Eight specific disorders related to central sensitization are suggested to be restless leg syndrome, chronic fatigue syndrome, fibromyalgia, temporomandibular disorder, migraine or tension headache, irritable bowel syndrome, multiple chemical sensitivities, and whiplash injury; non-specific emotional disorders related to central sensitization include anxiety or panic attack and depression. These central sensitization pain syndromes are overlapped to previous functional pain syndromes which are unlike organic pain syndromes and have emotional components. Therefore, nociplastic pain can be understood as chronic altered nociception related to central sensitization including both sensory components with nociceptive and/or neuropathic pain and emotional components. Nociplastic pain may be developed to explain unexplained chronic pain beyond tissue damage or pathology regardless of its origin from nociceptive, neuropathic, emotional, or mixed pain components.

One of the most common sources of spinal pain syndromes is the facet joints. Cervical, thoracic, and lumbar facet joint pain syndromes comprise 55%, 42%, and 31% of chronic spinal pain syndromes, respectively. Common facet joint disorders are degenerative disorders, such as osteoarthritis, hypertrophied superior articular process, and facet joint cysts; septic arthritis; systemic and metabolic disorders, such as ankylosing spondylitis or gout; and traumatic dislocations. The facet pain syndrome from osteoarthritis is suspected from a patient’s history (referred pain pattern) and physical examination (tenderness). Other facet joint disorders may cause radicular pain if mass effect from a facet joint cyst, hypertrophied superior articular process, or tumors compress the dorsal root ganglion.However, a high degree of morphological change does not always provoke pain. The superiority of innervating nerve block or direct joint injection for diagnosis and treatment is still a controversy. Treatment includes facet joint injection in facet joint osteoarthritis or whiplash injury provoking referred pain or decompression in mass effect in cases of hypertrophied superior articular process or facet joint cyst eliciting radicular pain. In addition, septic arthritis is treated using a proper antibiotic, based on infected tissue or blood culture. This review describes the diagnosis and treatment of common facet joint disorders.

PURPOSE: The purpose of this study was to compare the sliding distance of lag screw in patients with unstable femoral intertrochanteric fractures treated with intramedullary fixation using a cephalomedullary nail with a fixed angle between the neck and shaft of the femur in relation to reduction type by lateral radiographs. MATERIALS AND METHODS: Between January 2009 to October 2013, 86 cases (86 patients) with unstable femoral intertrochanteric fractures were treated with intramedullary fixation using a metal nail with a fixed neck-shaft angle and followed for at least 6 months. We used AO/OTA classification, and all cases were unstable fractures. Twenty cases were 31-A22, 54 cases were 31-A23, and 12 cases were 31-A3. There were 30 men and 56 women. Average patient age was 73.7 years (range, 47-97 years). We classified reduction types into three groups as postoperative lateral radiologic findings. Group 1 showed no displacement, group 2 showed anterior displacement of the femur neck, and group 3 showed posterior displacement of the femur neck. The radiological assessment compared the sliding distance of the lag screw between postoperative X-ray and last follow-up X-ray. RESULTS: Forty-two cases were in group 1, 22 cases were in group 2, and the other 22 cases were in group 3. There was no significant difference in the patient characteristics of each group. The sliding distances of the lag screw were 4.9±3.2 mm, 4.6±3.6 mm, and 8.5±4.9 mm, respectively, and group 3 showed a significant result (p<0.0001, p=0.024). CONCLUSION: In cases treated with intramedullary fixation using a cephalomedullary nail with a fixed neck-shaft angle, appropriate reduction with a lateral radiograph before screw fixation is needed to prevent excessive lag screw sliding.
Classification ; Female ; Femur ; Femur Neck ; Follow-Up Studies ; Fracture Fixation, Intramedullary ; Hip Fractures ; Humans ; Male ; Neck